Gonococci (Gc) are thought to require pilus+ for virulence, but pilus- status may also confer advantages on Gc in transmission to other hosts, spread in an individual, etc., if these organisms are capable of reversion to pilus+. In vitro, Gc display pilus+ pilus- "phase variation" at high frequency; at similarly high frequency, pilus+ GC also spawn variant pilus+ progeny that express structurally/antigenically distinct pili. Our current studies focus on the molecular mechanisms responsible for both phase and pilus structural changes. Work during the present year has documented gene conversion as accounting for both these changes in piliation. This occurs via non-reciprocal homologous recombination involving the Gc genome's single complete, expressed pilin structural gene and one of the multiple silent, storage partial pilin genes in the Gc chromosome. Whether pilus- or pilus+ phenotype obtains correlates with primary structure of the pilin polypeptide encoded by the newly constituted "chimeric" pilin gene resulting from the gene conversion event and whether that pilin polypeptide can or cannot form mature, polymeric pili. Other studies on recombination-deficient (rec-) Gc have defined spontaneous mutation (single nucleotide deletion/insertion/substitution) in the pilin structural gene as accounting for changes in piliation status. Among the mutants isolated is one in which mutational change in the last amino acid in the pilin polypeptide's "leader" segment renders the pilin- nonfunctional regarding pilus formation. Other piliation mutans in the rec- Gc include "ochre" mutants synthesizing a truncated pilin polypeptide. Examination of Gc emanating from a experimental human infection has documented changes in both pilin structure and in protein II constitutions of Gc isolated versus Gc inoculated.